01 Before - Vitamin D: what is it and how does it work in the body?

Vitamin D is a fat-soluble vitamin, and can be ingested or made by the body itself. Vitamin D3 is one of the two forms of vitamin D that can be ingested, along with vitamin D2. Vitamin D3 is mostly present in foods of animal origin (Borel, Caillaud, & Cano, 2015), and is taken up by the intestines and transported to the liver. In the liver, the vitamin D3 is converted by addition of an -OH group to the pre-hormone 25(OH)D or calcifediol. The calcifediol can then be converted to 1,25(OH)2D3 or calcitriol, the active form of vitamin D, in the kidneys. Once active, vitamin D can bind to vitamin D receptors (VDRs), which are present in nearly every nucleated cell of the human body (Ksiażek, Zagrodna, & Słowińska-Lisowska, 2019). After binding VDRs, vitamin D has positive effects on bone mineralization, the immune system, endocrine system, gene expression, and on the muscular system (Ogan & Pritchett, 2013). There is a distinction in endocrine and autocrine mechanisms that vitamin D3 elicit in the body. 

The endocrine function is related to bone growth, since vitamin D3 is essential for this growth (Willis, Peterson, & Larson-Meyer, 2008). Vitamin D has been shown to enhance intestinal calcium absorption and influences osteoclast activity (Ogan & Pritchett, 2013); osteoclasts are the cells that break down the bone. A shortage of vitamin D causes an increase in bone turnover, which leads to an increased risk for bone injuries (Ogan & Pritchett, 2013). The International Olympic Committee found low vitamin D status to be associated with a 3.6 time increased risk for stress fractures, and with supplementation of 20 μg/day combined with calcium, this risk decreased (Maughan et al., 2018). In short, vitamin D3 is essential for bone growth, and a shortage causes an increase in risk for stress fractures.

The other mechanism is the autocrine pathway. This pathway involves processes like gene expression, protein synthesis, cell synthesis, hormone synthesis, and immune responses (Ksiażek et al., 2019). The VDRs affect over hundreds of genes in the body that perform essential functions (Ksiażek et al., 2019). These receptors are also found in muscle tissue. A study showed that severely vitamin D-deficient patient’s muscle biopsies indicated an increase in the number and diameter of fast, type II muscle fibers with an increase in serum vitamin D (Cannell, Hollis, Sorenson, Taft, & Anderson, 2009). This conclusion was confirmed by others, who showed that vitamin D supplementation led to an increase in type II muscle fibers and their size (Chiang, Ismaeel, Griffis, & Weems, 2017; Ogan & Pritchett, 2013). Thus, vitamin D supplementation can induce an increase in type II muscle fibers and their size via VDRs found in muscle tissue.

Not only do the VDRs influence the muscle synthesis, VDRs are also found in most of the immune cells. 25(OH)D has been found to influence the activation of the immune system, by increasing the gene expression for antimicrobial peptides with an increased concentration (Ksiażek et al., 2019). These antimicrobial peptides are important for the innate immune system, and help battle acute infections. In addition, Willis et al. (2008) reported that VDRs regulate T- and B-lymphocyte function, cytokine production, macrophage activation, and monocyte maturation. Additionally, vitamin D has been shown to increase the production of anti-inflammatory cytokines transforming growth factor and IL-4 (Willis et al., 2008). In short, 25(OH)D increases the gene expression for antimicrobial peptides and VDRs regulate several important players of the immune system.

The above-mentioned effects of vitamin D3 are very interesting. However, worldwide, vitamin D deficiency is considered an epidemic for all age groups (Willis et al., 2008). This deficiency is defined as <20 ng/mL (50 nmol/L blood), insufficiency as 20–32 ng/mL (50–80 nmol/L blood) and optimal levels are >40 ng/mL (100 nmol/L blood) (Ogan & Pritchett, 2013). Not only is the general population at risk, athletes have equal risk for vitamin D insufficiency (Ogan & Pritchett, 2013). A large meta-analysis demonstrated that of 2313 professional athletes, 56% had an inadequate 25(OH)D concentration throughout the whole year, with the concentration being even lower in the winter months (Farrokhyar et al., 2015). Vitamin D deficiency may decrease strength and degenerate type II muscle fibers, which negatively correlates with physical performance (Ksiażek et al., 2019). Additionally, a deficiency may influence the immune system as well as increase the risk for stress fractures. In conclusion, vitamin D deficiency is a worldwide epidemic, which athletes are at an equal risk for.